Frequency of eosinophils expressing activation markers, PRRs and T-cell activation molecules in PCM patients (n = 12, black bars) and healthy controls (n = 8, white bars).

<p>Peripheral blood eosinophils were purified and incubated with antibodies against human CD69, TLR2, TLR4, MHC-II, CD80 and CD86 and the frequency of each population was evaluated by FACs. Results are expressed as mean ± SEM. <i>Student t test</i>: * p <0.05, ** p <0.01, *** p <0.001, compared to control cells.</p

Frequency of eosinophils expressing activation markers, PRRs and T-cell activation molecules in PCM patients (n = 12, black bars) and healthy controls (n = 8, white bars).

<p>Peripheral blood eosinophils were purified and incubated with antibodies against human CD69, TLR2, TLR4, MHC-II, CD80 and CD86 and the frequency of each population was evaluated by FACs. Results are expressed as mean ± SEM. <i>Student t test</i>: * p <0.05, ** p <0.01, *** p <0.001, compared to control cells.</p

Immunohistochemistry detection of chemokines and granule proteins in liver and lymph nodes from PCM patients.

<p>MBP (A,D), CCL5 (B,E) and CCL11 (C,F) were stained in cells distributed in inflammatory infiltrates of lymph nodes (LN) and liver from PCM patients (Original magnification x 400).</p

Relative migration of eosinophils of patients with PCM (n = 7–10, black triangle) and controls (n = 5–8, open circles) to CCL11 (100ng/mL), CCL5 (100ng/mL) and interleukin-5 (100 and 50 ng/ml).

<p>Eosinophils were maintained in the presence or not of <i>P</i>. <i>brasiliensis</i> yeasts (Pb18 or Pb265) for 4 hours, as indicated. Results are expressed as median. <i>Mann Whitney test</i> * p <0.05.</p

Serum concentration of EPO, ECP, EDN, MBP, CXCL9, CXCL10, CCL5 and CCL11 in patients (n = 13–16) with acute form of PCM and controls (n = 8–10).

<p>Results are expressed as median. <i>Mann Whitney test</i> * p <0.05.</p

Clinical characteristics of patients.

<p>Clinical characteristics of patients.</p

Number of eosinophils from patients with PCM (n = 5, black bars) and healthy controls (n = 6, white bars) adhering to human lung endothelial cells (HLECs).

<p>Eosinophils were pre incubated for 30 min with (A) culture medium (basal), (B) CCL11 (100ng/ml), (C) IL-5 (100ng/ml) or (D) CCL5 (100ng/ml) prior to incubation with HLECs for 1 hour. Results are expressed as mean ± SEM. <i>Student t test</i>: * p<0.05.</p

Brazilian guidelines for the clinical management of paracoccidioidomycosis

<div><p>Abstract Paracoccidioidomycosis is a systemic fungal disease occurring in Latin America that is associated with rural environments and agricultural activities. However, the incidence and prevalence of paracoccidiodomycosis is underestimated because of the lack of compulsory notification. If paracoccidiodomycosis is not diagnosed and treated early and adequately, the endemic fungal infection could result in serious sequelae. While the Paracoccidioides brasiliensis ( P. brasiliensis ) complex has been known to be the causal agent of paracoccidiodomycosis, a new species, Paracoccidioides lutzii ( P. lutzii ), has been reported in Rondônia, where the disease has reached epidemic levels, and in the Central West and Pará. Accurate diagnoses and availability of antigens that are reactive with the patients’ sera remain significant challenges. Therefore, the present guidelines aims to update the first Brazilian consensus on paracoccidioidomycosis by providing evidence-based recommendations for bedside patient management. This consensus summarizes etiological, ecoepidemiological, molecular epidemiological, and immunopathological data, with emphasis on clinical, microbiological, and serological diagnosis and management of clinical forms and sequelae, as well as in patients with comorbidities and immunosuppression. The consensus also includes discussion of outpatient treatments, severe disease forms, disease prevalence among special populations and resource-poor settings, a brief review of prevention and control measures, current challenges and recommendations.</p></div